Up-regulation of cyclooxygenase-2 gene expression by chorionic gonadotropin during the differentiation of human endometrial stromal cells into decidua

Han, S. W.

doi:10.1210/en.137.5.1791

Cited by 45 publications

(20 citation statements)

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“…Oestradiol downregulated this isoform in the bovine (Xiao et al 1998) and ovine (Charpigny et al 1997a) endometrium. A stimulatory effect of hCG on COX-2 in endometrial cells was reported in women (Han et al 1996). Moreover, LH increased COX (measured as both isoforms; Stepien et al 1999) and COX-2 (A.…”

Section: Discussionmentioning

confidence: 88%

Expression of Cyclooxygenase‐1 and ‐2 in the Porcine Endometrium during the Oestrous Cycle and Early Pregnancy

Blitek

Wacławik

Kaczmarek

et al. 2006

Reprod Domestic Animals

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Cyclooxygenase (COX) is the rate-limiting enzyme that catalyses the initial step in prostaglandins (PGs) production. In the present studies, endometrial COX-1 and COX-2 expression throughout the oestrous cycle and early pregnancy was analysed in pigs using real-time reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot and immunohistochemistry. There were no changes in messenger RNA (mRNA) and protein expression for COX-1 in cyclic pigs. In pregnant animals, mRNA levels of this enzyme increased on days 22-25 (p < 0.001). However, no upregulation of COX-1 protein was detected. Quantification of COX-2 mRNA expression during the oestrous cycle revealed significant increases on days 10-12 and 14 (p < 0.001 and p < 0.01 vs days 2-4, respectively). Protein levels were also increased on day 14 when compared with days 2-12 and 18-20 after oestrus. In pregnant animals, the patterns of both COX-2 mRNA and protein expression were similar. Messenger RNA levels were higher on days 16 and 22-25 (p < 0.01 vs day 10). Moreover, the protein content tended to increase on days 16 and 22-25. COX-1 and COX-2 were localized in the luminal and glandular epithelium as well as in the uterine stroma. In contrast to COX-1, a positive immunostaining reaction for COX-2 was detected only on days 12-16 after ovulation and on days 14-16 of pregnancy. In conclusion, these results indicate specific patterns of COX-1 and COX-2 expression in the porcine endometrium throughout the oestrous cycle and early pregnancy. COX-2 rather than COX-1 seems to be the primary enzyme responsible for modulated PGs production at the time of luteolysis in cyclic and during implantation in pregnant animals.

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Section: Discussionmentioning

confidence: 88%

Expression of Cyclooxygenase‐1 and ‐2 in the Porcine Endometrium during the Oestrous Cycle and Early Pregnancy

Blitek

Wacławik

Kaczmarek

et al. 2006

Reprod Domestic Animals

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“…Western blotting was performed as previously described [15]. Briefly, protein concentrations were determined by the Bio-Rad protein assay.…”

Section: Methodsmentioning

confidence: 99%

Rosiglitazone, an Agonist of PPARγ, Inhibits Non-Small Cell Carcinoma Cell Proliferation In Part through Activation of Tumor Sclerosis Complex-2

Han

Zheng²,

Roman³

2007

PPAR Research

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PPARγ ligands inhibit the proliferation of non-small cell lung carcinoma (NSCLC) cells in vitro. The mechanisms responsible for this effect remain incompletely elucidated, but PPARγ ligands appear to inhibit the mammalian target of rapamycin (mTOR) pathway. We set out to test the hypothesis that PPARγ ligands activate tuberous sclerosis complex-2 (TSC2), a tumor suppressor gene that inhibits mTOR signaling. We found that the PPARγ ligand rosiglitazone stimulated the phosphorylation of TSC2 at serine-1254, but not threonine-1462. However, an antagonist of PPARγ and PPARγ siRNA did not inhibit these effects. Rosiglitazone also increased the phosphorylation of p38 MAPK, but inhibitors of p38 MAPK and its downstream signal MK2 had no effect on rosiglitazone-induced activation of TSC2. Activation of TSC2 resulted in downregulation of phosphorylated p70S6K, a downstream target of mTOR. A TSC2 siRNA induced p70S6K phosphorylation at baseline and inhibited p70S6K downregulation by rosiglitazone. When compared to a control siRNA in a thymidine incorporation assay, the TSC2 siRNA reduced the growth inhibitory effect of rosiglitazone by fifty percent. These observations suggest that rosiglitazone inhibits NSCLC growth partially through phosphorylation of TSC2 via PPARγ-independent pathways.

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“…Western blotting detection of HIF-1α and DEC1 Western blotting was performed as previously described with some modifications [20] . The cell pellets were homogenized in extraction buffer (50 mmol/L Tris-HCl, pH6.8, 0.1% SDS, 150 µmol/L NaCl, 100 mg/L phenylmethylsulfonyl fluoride, 1 mg/L aprotinin, 1% NP-40 and 0.5% sodium orthovanadate), and incubated at 4 °C for 30 min, and centrifuged 20 min at 12 000 g/min.…”

Section: Rt-pcr Detection Of Dec1 and Hif-1αmentioning

confidence: 99%

Embryo-chondrocyte expressed gene 1, downregulating hypoxia-inducible factor 1?, is another marker of lung tumor hypoxia

Zhang

2007

Acta Pharmacologica Sinica

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Aim: To explore the mechanism of differentiated embryo-chondrocyte expressed gene 1 (DEC1) in the lung adenocarcinoma A549 cell line and its relationship with hypoxia-inducible factor 1α (HIF-1α). Methods: DEC1 and HIF-1α protein levels were detected in lung adenocarcinoma tissues by immunohistochemistry. A549 cells were cultured at hypoxia. MTT assay was used to determine the effect of cell viability. The apoptotic analysis was determined by flow cytometry. RT-PCR and immunocytochemistry were carried out to observe the DEC1 and HIF-1α mRNA and protein expression. HIF-1α mRNA and protein levels were detected in the stably transfected pcDNA-DEC1+/-A549 cells by RT-PCR and Western blotting. DEC1 mRNA and protein levels were detected in the stably transfected pcDNA-DEC1+/-A549 cells with or without HIF-1α antisense oligonucleotide treatment by RT-PCR and Western blotting. Results: DEC1 was specifically located in 40 (48.8%) lung adenocarcinoma tissues. The results of the MTT test showed the growth of the stably transfected pcDNA-DEC+ A549 cells was higher than those of A549 cells and the stably transfected pcDNA-DEC-A549 cells. Hypoxia also induced the apoptosis of A549 cells and the stably transfected pcDNA-DEC+/-A549 cells. Hypoxia increased the mRNA and protein levels of DEC1 and HIF-1α. Both HIF-1α mRNA and protein levels decreased in the stably transfected pcDNA-DEC+ cells, but HIF-1α antisense oligonucleotide had no effect on DEC1 in the stably transfected pcDNA-DEC+/-A549 cells. Conclusion: DEC1 is a marker of tumor hypoxia. DEC1 downregulates the HIF-1α at both mRNA and protein levels at hypoxia in lung adenocarcinoma A549 cells.

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Up-regulation of cyclooxygenase-2 gene expression by chorionic gonadotropin during the differentiation of human endometrial stromal cells into decidua

Cited by 45 publications

References 0 publications

Expression of Cyclooxygenase‐1 and ‐2 in the Porcine Endometrium during the Oestrous Cycle and Early Pregnancy

Expression of Cyclooxygenase‐1 and ‐2 in the Porcine Endometrium during the Oestrous Cycle and Early Pregnancy

Rosiglitazone, an Agonist of PPARγ, Inhibits Non-Small Cell Carcinoma Cell Proliferation In Part through Activation of Tumor Sclerosis Complex-2

Embryo-chondrocyte expressed gene 1, downregulating hypoxia-inducible factor 1?, is another marker of lung tumor hypoxia

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